Comparison of plasma concentrations of thromboxane B2 in prinzmetal's variant angina and classical angina pectoris

Clinical Cardiology - Tập 2 Số 6 - Trang 404-406 - 1979
Robert Ira Lewy1,2, Leslie Wiener1, J B Smith1, Paul Walinsky1, Melvin J. Silver1, John Saia1
1Cardeza Foundation for Hematologic Research, Division of Cardiology and Department of Pharmacology, Thomas Jefferson University, Philadelphia, Pennsylvania, USA
2Training Grant AM-07084

Tóm tắt

AbstractWe have reported that thromboxane B2 is present in plasma of Prinzmetal's angina patients measured by radioimmunoassay but is below detection limits, <0.5 pmol/ml, in normals. To determine whether this metabolite of thromboxane A2 (a coronary vasoconstrictor) is present in the peripheral blood in classical angina pectoris, we studied 14 patients with fixed obstructive coronary artery disease (2.5 lesions per patient) in whom angina was induced by atrial pacing. Thromboxane B2 at rest was barely detectable (0.537±0.16 pmol/ml), but rose during pacing (0.747±0.18 pmol/ml) and was maximal (p<0.05) 5–10 min after pacing (1.237±0.36 pmol/ml). In eight variant angina patients, resting levels of thromboxane B2 were not statistically different during spontaneous angina and angina‐free intervals (2.837±0.56 and 1.577±0.34 pmol/ml), but the mean 5–10 min after angina was higher than during angina (6.41 7±1.46 pmol). The means of preanginal, anginal, and postanginal samples were all higher than the corresponding means of the classical angina group, and thromboxane B2 levels in variant angina patients in the absence of angina, during angina, and 5–10 min after angina were all significantly higher (p<0.025) compared to the classical angina group measured prior to pacing. Unlike the case with variant angina, thromboxane B2 is indetectable in classical angina pectoris patients at rest. Furthermore, spontaneous angina in variant angina or pacing‐induced angina in classical angina pectoris are both followed by increased thromboxane B2, although the latter responses are smaller. The role of these phenomena in the pathogenesis of coronary artery spasm and ischemia remains to be clarified.

Từ khóa


Tài liệu tham khảo

10.1016/S0090-6980(74)80130-9

Bills TK, Metabolism of 14C‐arachidonic acid by human platelets, Biochim Biophys Acta, 424, 303, 10.1016/0005-2760(76)90198-3

Caldwell BV, Development and application of a radioimmunoassay for F prostaglandins, J Reprod Med, 9, 361

Ellis EF, Coronary arterial smooth muscle contraction by a substance released from platelets. Evidence that it is thromboxane A2, Science, 193, 1135, 10.1126/science.959827

Ferraris V, Radioimmunoassay of thromboxane B2, Thromb Haemostasis, 38, 20

10.1073/pnas.72.8.2994

Hillis LD, Coronary artery spasm, N Engl J Med, 229, 695

Kindahl H, Metabolism of thromboxane B2 in the cynomolgus monkey, Prostaglandins, 13, 619, 10.1016/0090-6980(77)90233-7

10.1016/0161-4630(79)90059-4

10.1126/science.945611

Ogletree ML, 1978, Actions of prostaglandins on isolated perfused cat coronary arteries, Am J Physiol, 235, H400

Snedecor W, 1967, Statistical Methods, 205

10.1038/274064a0

10.1016/0090-6980(76)90128-3

Wiener L, 1978, Therapeutic implications of myocardial lactate metabolism in patients considered for emergency myocardial revascularization, J Thorac Cardiovasc Surg, 75, 612, 10.1016/S0022-5223(19)41250-6

Thông tin
Thông tin xuất bản

Clinical Cardiology

Tập 2 Số 6

404-406

Thông tin tác giả